An intriguing therapeutic target
Degenerative anatomical changes in the trabecular meshwork (TM) may limit trabecular outflow, leading to the elevated intraocular pressure (IOP) seen in glaucomatous eyes.1-4
Changes in the TM detected using scanning electron microscopy (x2000)3
Normal TM (left), Primary open-angle glaucoma (POAG) TM (right)
The potential consequences of limiting trabecular outflow
The avascular TM relies on the flow of aqueous humor for nutrients, growth factors, and antioxidants. Anything that limits this flow through the TM could promote further anatomical changes.2
Dysfunction at the trabecular meshwork and glaucoma: Restricted outflow through the TM and fibrosis in the tissue may be key to the underlying pathophysiology of glaucoma.
1. Goel M, Picciani RG, Lee RK, Bhattacharya SK. Aqueous humor dynamics: a review. Open Ophthalmol J. 2010;4:52-59. 2. Kopczynski CC, Epstein DL. Emerging trabecular outflow drugs. J Ocul Pharmacol Ther. 2014;30(2-3):85-87. 3. Sacca SC, Pulliero A, Izzoti A. The Dysfunction of the Trabecular Meshwork During Glaucoma Course. J Cell Physiol. 2015;230:510-525. 4. Sihota R, Goyal A, Kaur J, Gupta V, Nag TC. Scanning electron microscopy of the trabecular meshwork: Understanding the pathogenesis of primary angle closure glaucoma. Indian J Ophthalmol. 2012;60(3):183-188.